ARDS

Question 1

Define ARDS

Answer 1

Acute non cardiogenic pulmonary oedema that occurs after various systemic or local insults. Respiratory disorder that meets four general clinical criteria

1) acute onset
2) poor oxygenation
3) bilateral chest radiographic infiltrates
4) conditions that are unexplained by CCF or overload

Question 2

Discuss pathogenesis of ARDS

Answer 2

Results from injury to the alveolar-capillary membrane that is caused by exogenous agents or be endogenous inflammatory mediators
This injury results in leakage of plasma into the lungs interstitial and alveolar space with the result of alveolar flooding and eventual resp failure

Question 3

Discuss causes for ARDS

Answer 3

Direct damage

• aspiration pneumonia
• pneumonia regardless of etiology
• smoke or toxic gas inhalation
• primary gragt dysfunction post transplant
• near drowning

Indirect causes of lung injury

• acute pancreatitis
• fulminant hepatic failure
• massive blood transfusion with TRALI
• severe trauma without lung contusion, but especially with broken ribs or fat emboli
• postcardiopulmonary bypass
• severe sepsis and septic shock

Question 4

Discuss clinical features of ARDS

Answer 4

Present with respiratory distress at the same time or shortly after precipitating event. Rapid shallow breathing with or without crepitations and characteristically bilateral infiltrates without cardiac enlarement

ABG shows hypoxia and intially hypocarbia and respiratory alkalosis. Pao2 will remain low secondary to shunting from flooded alveolar despite oxygen supplementation. Type 2 resp failure will develop with fatigue and patient will need to be ventilated

Question 5

Discuss mechanisms of lung injury in ARDS

Answer 5

Early phase (exudative)

• presents as lung failure alone or failure of lungs with failure of other organs as part of a multiorgan system failure (MOSF)
• initially nil chagnes seen apart from interstital odeme resulting from alveolar capillary barrier dysfunction
• after gross alveoalr oedema forms a pattern of diffuse alveolar damagge is opresent

Fibroproiferative phase (late)

• in those who survive early phase alveolar and interstial remodeling occur. can occur as early as 1 week after initial insult
• type 2 pneumocyte proliferate and differentiate into typ1 to reconstitute the alveolar epithelium
• fibroblast proliferate and lead to interstitial fibrosis
• O2 toxicity may exacerbate this

Question 6

Discuss pathophys of ARDS (hypoxia)

Answer 6

In early phase of ARDS the most life-threatening problem is hypoxia.
This results from a large right to left shunt as blood passes through flooded alveolar

Can estimate shunt volume as 5% shunt for every 100mghg of O2 from 700mghg when breathing fio2 1
those requiring ventilation usually have shunts ranging from 25-50%

Resistant to o2 supplementation due to shunt so goal is to reduce shunt volume by opening flooded alveoli i:e alvoali whose V/Q is 0

Question 7

Discuss pathophys of ARDS (compliance)

Answer 7

decrease compliance is due to widespread interstitial and alvolar oedema and atelectatic alveoli.
Decreased surfactant activity leads to the collapse of alveoli at end-expiration and increased hystersis

at least 3 mechanisms are involved in reduced surfactant

1) flooding of alveolar washes out surfactant
2) destruction of type 2 pneumocytes reduces production and secretion
3) contact with plasma proteins inactivates surfactant

Question 8

Discuss pathophys of ARDS (minute ventilation)

Answer 8

Patient with ARDS have an increased minute ventilation
This is due to an increase in V/Q mismatching from flooded alveolar
Can have VT/VD ratio in the range of 0.7-0.8 where as normal is 0.3
need to increase MV by up to three time to maintain co2 excretion
During mechanical ventilation this requires high flow rates to keep I:E ratio <1

need high RR to maintain normocarbia and low TV this can lead to short expiratory phase and increasing intrinsic PEEP and dynamic overinflattion. May need permissive hypercapnia in this regard

Question 9

Discuss specific management for ARDS

Answer 9

Directed against the cause of ARDS
Limited in less the causes is a treatable infection or ARDS resulting from diffuse pulmonary haemorrhage
Suggestion of high dose steroids but nil consensus so not recommended
The current approach is to focus on a variety of supportive measures

Question 10

Discuss supportive management of ARDS

Answer 10

1) mechanical ventilation
- nearly all patients with ARDS will require ETT and mechanical ventilation
- aiming for Pao2 of 55mghg to80
- non toxic levels of inspired o2 (assumed to be 0.5-0.6)
- protecting lung from ventilator induced injury

2) low tidal volume ventilation
- should decrease alveolar overdistention and associated alveolar injury

3) PEEP
- improves arterial oxygenation and decreases right to left shunt
- PEEP increases functional residual capacity of the lung by re-inflating completely atelectatic alveoli and expanding partially etelectatic alveolar
- improves compliance and reduce number of alveoli with V/Q of close to 0 or 0
- increasing PEEP may decrease CO but decreasing preload , can reverse with inotropes and fluid loading but the latter can worsen alveolar oedema

Question 11

Discuss rescue therapies for refractory hypoxemia

Answer 11

1) prone positioning
- rationale is based on CT finding in ARDS that show localization of lung water in the dependant part f the lung.
- theorised that positioning the patient prone would reduce right to left shunt
- improved oxygen has been shown but nil improvement in mortality

2) inhaled NO and epoprostenol
- vasodilator
- is inhaled only to open alveolar causing preferential vasodilation in these areas with increased blood flow to ventilated areas reducing v/q mismatch

3) neuromuscular blockade
4) ECMO

4) haemodynacmic, fluid and diuretic therapy
- diuretic and fluid restriction can low pulmonary capillary pressure, in patient with MOSF this is limited by hypoperfusion